Function of protein kinase C (PKC) in the regulation of apoptosis related hyperglycemia in vascular smooth muscle cells.

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Atherosclerosis is accelerated by the coexistence of diabetes mellitus. Hyperglycemia is an important etiologic factor in the development of vascular complications.(1) Effect of high glucose on cell proliferation and apoptosis in vascular smooth muscle cells (VSMC).High glucose stimulated cell proliferation and suppressed induction of apoptosis significantly in VSMC.(2) Effect of overexpression of PKC isozyme on cell proliferation and apoptosis in VSMC.Overexpression of PKC-βI stimulated cell proliferation and inhibited apoptosis expression in VSMC.In contrast, Overexpression of PKC-βII inhibited cell proliferation and increased induction of apoptosis in VSMC.(3) Effect of high glucose on the expression of PKC isozymes and apoptosis-related proteins, Bcl-xL and Bfl-1/A1.Treatment with a high glucose caused a significant decrease in apoptosis in CASMC compared with the same cells treated with a physiologically normal glucose concentration. Treatment of CASMC with high glucose concentration markedly increased mRNA expressions of bcl-xL and bfl-1/A1 compared with cells treated with normal glucose. High glucose suppressed apoptosis via upregulation of bcl-xL and bfl-1/A1 levels. High glucose-induced increase in the expression of antiapoptotic proteins may be important in the development of atherosclerosis in diabetic patients.